RATIONALE OF ENDO TREATMENT usefulness and advantages

rationale of endo treatment

2. The word “Rationale” means
fundamental reason or logical basis.
The rationale of endodontic treatment is
based on the belief that the natural
teeth function more efficiently than a
bridge ,partial denture or a metal
implant.

3. Endodontic treatment allow the removal of
vital or necrotic pulp from the canal system
of an infected tooth and replacement of
this space by an inert filling material.
This is mainly done to prevent extension of
the disease from pulp into periapical tissues
or where it has already occurred ,to
encourage resolution and return into
normal

4. 1.1890- Dentist and the physician ,W.D. Miller
associated the presence of bacteria in
pulpal and periapical disease.
2.1891- WD Miller, described human mouth as
focus of infection and recommend for
treating and filling the root canals.

5. 1909- E.C Rosenow described the
“Theory of focal infection.”
A localized or generalized infection caused
by bacteria travelling through the blood
stream from a distant focus of infection.

6. Treatment of pulp related pathosis
COMPOSITION OF THE PULP
Cells Fibers Ground substance
Odontoblasts
Fibroblasts
Undifferentiated
mesenchymal cells
Macrophages
Immunocompetent
cells
Collagen –
Type I
Type III
Oxytalan
Water
Glycosaminoglyca
ns
Glycoproteins
Proteoglycans

8. 1.Bacterial
2.Traumatic
3.Chemical
4.Idiopathic

9. Mild to moderate
›sclerosis
›Reparative dentin
›Reversible inflammation
Severe
›Irreversible changes
›Necrosis
›Periradicular pathosis

12. Clear understanding of inflammation is
important to understand the disease
process
Inflammation is a local physiological
reaction of the body to various stimuli or
irritants.
The objective of inflammation is to remove
or destroy the irritants and repair of the
damage to the tissues.

13. Inflammation produces the following symptoms:
 Pain, from the action of cytotoxic agents released
from humoral, cellular, and microbial elements on
the nerve endings
 Swelling, produced by filtration of macromolecules
and fluids into the affected tissues
Redness
Heat, produced by vasodilatation of the vessels
and the rushing of blood to the affected tissues
Disturbance of function, resulting from changes in
the affected tissues

14. Acute inflammation -Polymorphonuclear
neutrophils
Chronic inflammation - Monocytes
- Macrophages
- Lymphocytes
- Plasma cells
Other cells - Eosinophils
- Basophils
-mast cells

15. The polymorphonuclear neutrophils morphologically
consist of a nucleus with three or more connected
lobules and cytoplasm containing lysosomal and
specific granules.
They are present during the acute or early stages of
inflammation, and although their main function is to
phagocytize bacteria, they may also phagocytize and
lyse fibrin and cellular debris.
They are attracted to the area of inflammation by
chemotactic factors produced by bacteria or by
complement. Serum factors of complement and
immunoglobulins called opsonins bind bacteria to the
surfaces of the polymorphonuclear neutrophils.
Polymorphonuclear Neutrophils

16. In the binding sites, the bacteria are
encapsulated in vacuoles that move
into the cytoplasm of the
polymorphonuclear neutrophils and
come in contact with the lysosomal
granules. These lysosomal granules
degranulate and release lysosomal
enzymes inside the vacuoles for lysis of
the bacteria.

17. The polymorphonuclear neutrophils have a narrow range
of life; they are destroyed in the inflammatory site when
the tissue fluids fall to a pH of 6.5.
This tissue change is due to the increased production of
lactic acid during phagocytosis and the release of this
product into the tissues during the death of the
polymorphonuclear neutrophils.
Destruction of the polymorphonuclear neutrophils also
causes the release of the proteolytic enzymes pepsin and
cathepsin, with resulting tissue lysis.
The polymorphonuclear neutrophils, with the products of
cellular lysis and debris, are the principal constituents of
pus.

18. Macrophages are derived from
circulating monocytes. Immature
monocytes in extravascular areas, such as
areas of inflammation, differentiate into
macrophages. Macrophages are
phagocytic cellsthat ingest cellular debris,
microorganisms, and particulate matter.
They secrete certain mediators of
inflammation, such as lysosomal enzymes,
complement proteins, and prostaglandins.

19. Macrophages enhance the immunologic
reaction by ingesting, processing, and
degrading antigen before it is presented
to the lymphocytes. Their capacity to
remove debris from the area facilitates
repair. Macrophages are mononucleated
cells that, in periods of great activity, may
fuse with other macrophages to produce
a multinucleated giant cell.

20. Small lymphocytes appear in the chronic stage of the
inflammatory reaction. These lymphocytes are intimately
related to the immunologic system of the organism. Small
lymphocytes have a large, spherical, or slightly indented
nucleus surrounded by a thin band of cytoplasm
containing small granules.
Two types of small lymphocytes, B cells and T cells, are
known. Both are derived from the pluripotential
hemopoietic stem cells. Stem cells are carried by the
blood to the thymus, where they become immunologically
competent T cells. B cells, in contrast, are believed to
become immunocompetent in the bone marrow

21. T cells have a long life span and are the most
common cells of the lymphocytic series in
the blood. They are responsible for cell-
mediated immunity and for the
immunosurveillance of the human organism.
They recirculate through the lymphoid tissues
and organs of the body, except the thymus,
and are found in the paracortical areas of
the lymph nodes. When T cells are stimulated
by an antigen, a foreign substance, they
develop into sensitized T lymphocytes

22. These T lymphocytes have various
immunologic manifestations as follows:
Memory T cells, which speed the
immunologic reaction in subsequent
encounters with the same antigen
Helper or suppressor T cells, which stimulate
or suppress the development of effector T or
B cells
 Effector T cells, which may produce
cellmediated immune reactions, such as
delayed hypersensitivity

23. The sensitized T lymphocytes also release
chemical mediators called lymphokines.
Lymphokines may activate
macrophages, polymorphonuclear
leukocytes, and nonsensitized T cells, or
they may produce interferon, which
inhibits viral replication as needed by the
immune response.

24. B cells have a shorter life span than T cells.
They are found in the blood in lesser numbers
than T cells and in the cortical areas of the
lymph nodes. When activated by an antigen,
B cells become larger cells, called
plasmablasts, which divide to form plasma
cells and memory B cells. The memory B cells
speed the immunologic reaction in
subsequent encounters with the same
antigen. The B cells are responsible for the
humoral immunity of the human organism.

25. The plasma cells are large, oval, or round
cells with eccentric nuclei containing
chromatin arranged in cartwheel form. The
plasma cells produce immunoglobulins.
Immunoglobulins are called antibodies when
the antigen that triggers their production is
known. The immunoglobulins, of which the
five major classes are IgM, IgG, IgA, IgD, and
IgE, are involved in different defense
reactions.

26. These reactions include the following: y
Neutralization of bacterial toxins by
antitoxins y Coating of bacteria by
antibodies, or opsonization, to facilitate
phagocytosis y Lysis of bacteria by
complement activation y Agglutination
of bacteria y Combining of the antibody
with viruses to prevent their entry into the
cells

27. Other cells found in the pulp and periradicular
tissue during the inflammatory response are
eosinophilic leukocytes, basophilic leukocytes, and
mast cells. The eosinophils are found in allergic and
parasitic reactions. During the immune response,
they are involved in phagocytosis of the antigen–
antibody complexes and detoxification of
histamine. Basophils and mast cells are considered
similar cells; basophils are found in the hemopoietic
system and mast cells are found in tissue

28. They both contain granules that, when
stimulated by tissue injury or antigen,
degranulate and release chemical
mediators, such as histamine, a
vasodilator, and heparin, an
anticoagulant which can initiate an
inflammatory or allergic response.

29. Cytokines are low-molecular-weight
proteins that stimulate or inhibit the
proliferation, differentiation, or function of
immune cells. They play an important role in
modulating the inflammatory response of
the immune system.
Proinflammatory cytokines, e.g., TNF α, IL-1,
and IL-6
Anti-inflammatory cytokines, e.g., IL-4, IL-5,
IL-10, and IL-13

30. Injury, regardless of the cause or
intensity, causes two fundamental
vascular changes:
Vasodilatation
Increased capillary permeability, which,
in turn, leads to a series of interrelated
physiologic and morphologic changes
characteristic of the inflammatory
response

31. Physical, chemical, or biological irritation to
the pulp
Inflammatory changes
Protective mechanisms
Removal of the irritant
and/or therapeutic measures
Healing, leading to normal pulp
Vicious cycle of
inflammation
Persistence of
irritating factors

32. Protective Mechanisms in Limiting the Pressure Increase
within the Affected Pulp ƒ
The locally increased pressure in the inflamed area will
favor net absorption of interstitial fluid from adjacent
capillaries in uninflamed tissues. ƒ
Increased interstitial fluid pressure increases lymphatic
drainage. ƒ
Increased interstitial fluid pressure will lower the
transcapillary hydrostatic pressure difference and
oppose further filtration. ƒ
Discontinuity in the endothelium and fenestration of
pulpal capillaries may facilitate exchange mechanisms.
ƒ
Proper functioning of the feedback mechanisms will
limit the increased tissue fluid pressure to the affected
area, corresponding to that shown histopathologically

33. Irritation (Dental caries, trauma or operative procedures)

Localized inflammation
 
Vasodilatation
 
Increased local tissue pressure
Localized necrosis
 
Venous collapse
 
Reduced blood flow
 
Waste product accumulation
Progression of inflammation
 
Wider zone of inflammation
 
Spread of vascular disturbance
Generalized necrosis
 
Necrosis of additional tissue
 
Release of lysozomal enzymes
 
Extensive collagen destruction
Irreversible pulpitis

34. If the inflammatory response overwhelms the pulp, with
resulting partial or total necrosis, the root canal will serve as a
pathway to the periradicular area for the noxious products of
tissue necrosis and antigenic agents.
The inflammatory and immunologic responses in the
periradicular area occur as in the pulp.
On reaching the periradicular area, these noxious products cause
bone resorption and initiate the formation of granulation
tissue in place of normal periradicular tissues.
The periradicular pathologic tissues contain polymorphonuclear
neutrophils, lymphocytes, plasma cells, macrophages, and
mast cells, along with immunoglobulins IgG, IgA, IgM, and
IgE, and complement

35. In the presence of inflammatory cells,
immunoglobulins, and complement in the
periradicular tissues, anaphylactic, cytotoxic,
antigen–antibody complex, and delayed
hypersensitivity reactions may occur.
Reports indicate that some endodontic flareups are
mediated by IgE reactions and that bone resorption is
mediated by a lymphokine called osteoclast-
activating factor.
These findings point to the important role that
immunologic reactions play in the physiology and
pathology of the periradicular tissues

36. Tissue changes following inflammation
are either degenerative or proliferative.
Degenerative Changes
Degenerative changes in the pulp may
be one of the following:
Fibrous
Resorptive
Calcific

37. If the degeneration continues, necrosis will result, especially
if thrombosis of the blood vessels occurs, or if leukotoxin is
released as a result of damage to the tissue cells. Another
form of degeneration is suppuration.
When the polymorphonuclear cells are injured, they release
proteolytic enzymes, with resulting liquefaction of the dead
tissue. This process is suppuration or formation of pus
Three requisites are necessary for suppuration:
Necrosis of tissue cells
A sufficient number of polymorphonuclear
leukocytes
Digestion of the dead material by proteolytic
enzyme

38. Proliferative changes are produced by
irritants mild enough to act as stimulants.
Within the same area, a substance may be
both an irritant and a stimulant, such as
calcium hydroxide and its effect on adjacent
tissue.
In the center of the inflammatory area, the
irritant may be strong enough to produce
degeneration or destruction, whereas at the
periphery, the irritant may be mild enough to
stimulate proliferation.

39. Generally, if the tissue is in apposition, as in the case of an
incision for root resection, fibroblastic repair will take place.
When a gap is present between the tissue parts, repair is made
with granulation tissue.
Granulation tissue is resistant to infection. The principal cells
of repair are the fibroblasts which lay down cellular fibrous
tissue.
In some cases, collagen fibers may be substituted; dense
acellular tissue is then formed. In either case, fibrous repair is
the result. Destroyed bone is not always replaced by new
bone, but it may be replaced by fibrous tissue.

40. The reaction of the periradicular tissues
to noxious products of tissue necrosis,
bacterial products, and antigenic
agents from the root canal has been
described by Fish.

41. Zone of Irritation
Zone of Contamination
Zone of Stimulation
Zone of Necrosis

42. The reaction of the periradicular tissues to
noxious products of tissue necrosis,
bacterial products and antigenic agents
from the root canal has been established
by Fish who established experimental foci
of infection in the jaws of guinea pigs by
drilling openings in the bone and packing
in wool fibers saturated with a broth culture
of microbes.

43. Four well defined zones of reaction were found: 
1)Zone of Infection -
This zone is characterized by PMNs. Infection is
present is the center and microbes are found
only in this area.
2) Zone of Contamination -
This zone has inflammatory cells mostly but no
bacteria.this zone is around the central zone
with round cell infiltrate and cellular
destruction not from the bacteria themselves
but from toxins discharged from the central
zone.

44. 3) Zone of Irritation
This zone is characterized by histiocytes and
osteoclasts. It marks an area of bone resorption.
Collagen framework is digested by the
macrophages and the bone is resorbed by
osteoclasts. This causes a gap between the zone of
infection and the normal tissue. 
4) Zone of Stimulation
This area is characterized by fibroblasts osteoblasts.
Here the toxins are very mild enough to be a
stimulant. In response to this collagen fibers are laid
down by fibroblasts which act both as wall of
defense around the zone of irritation and as a
scaffold on which new osteoblasts build new bone.

45. Apical periodontitis is a body defence
response to the distruction of the pulpal
tissue and microbial infection of the root
canal system.
Microorganisms exists in the infected and
necrotic root canal system mostly as the
biofilms and also as aggregrates and
coaggregates.

46. The clash of the microbial and host
defense forces destroys much of the
periapical tissues
Results in apical periodontal lesions which
are generally barricated in dense
collagenous capsules.

47. Although this defensive reaction minimizes
the spread of the infection ,it cannot
eliminate microbes that are well
entrenched in the necrotic root canal as
protected biofilms.
Clinician must kept in mind therefore that
apical periodontitis is not self-
healing;resolution requires surgical and non
surgical endodontic therapy.

48. Steps:
formation and organization of a fibrin clot

granulation tissue formation and maturation

Subside of inflammation
restoration of normal architecture of the
periodontal ligament.

49. There will be formation of bony trabeculae
extending inward from the walls of the lesion
toward the root surface.
On the periphery, osteoblasts appear and
elaborate bone matrix (osteoid),which
gradually mineralizes as it matures.

50. If cementum or dentin has been
resorbed by the inflammation,
remodeling and repair by secondary
cementum
The last to form is likely the fibrous
component interposed between newly
formed bone and the cemental root
surface..

51. For the high standard treatment and
successful outcome without causing any
harm to the patient ,an endodontist
must understand the “why”and “how” of
the treatment procedure for which the
understanding of rationale is very
important.